The data of Cannon and co-workers on UCP1-ablated mice are interpreted assuming that UCP2 and UCP3 are involved in thermoregulation as fatty acid-dependent uncouplers although they are not sufficient, in the absence of UCP1, for long term maintenance of normal body temperature of mice after sudden and strong decrease in the ambient temperature. I would like to suggest that in brown fat of control mice, UCP1 is present in an amount higher than UCP2 and 3 and, therefore, is able to cause (a) some fatty acid-mediated decrease in proton motive force in resting state and, hence, (b) oxidation of CoQH2 to CoQ which is shown by Klingenberg and coworkers to be cofactor for UCPs. This results in strong uncoupling and thermogenesis mediated by UCP1, 2 and 3. In the UCP1-ablated mice, activity of UCP2 and 3 appears to be insufficient to induce CoQH2 oxidation in resting brown fat mitochondria, which results in hypothermia.
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April 01 2001
Barbara Cannon's Data on the UCP1-Ablated Mice: “Non-Cannonical” Point of View
Vladimir P. Skulachev
Vladimir P. Skulachev
1Department of Bioenergetics, A. N. Berlozersky Institute of Physico-Chemical Biology, Moscow State University, Moscow 119899, Russia
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Publisher: Portland Press Ltd
Online ISSN: 1573-4935
Print ISSN: 0144-8463
© 2001 Plenum Publishing Corporation
2001
Biosci Rep (2001) 21 (2): 189–194.
Citation
Vladimir P. Skulachev; Barbara Cannon's Data on the UCP1-Ablated Mice: “Non-Cannonical” Point of View. Biosci Rep 1 April 2001; 21 (2): 189–194. doi: https://doi.org/10.1023/A:1013600325266
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